HIF1A and experimental autoimmune encephalomyelitis: Suppressing HIF-1α-dependent glycolysis could impede the development of Th17 cells and delay the progression of experimental autoimmune encephalomyelitis (25, 26); therefore, we speculate that manipulation of HIF-1α and glycolysis may also be a potent way to relieve the psoriasis induced by γδ17 T cells.